Associations of metabolically healthy obesity with prevalence and progression of coronary artery calcification: Results from the Heinz Nixdorf Recall Cohort Study

Background and aims

There is controversy on the potentially benign nature of metabolically healthy obesity (MHO), i.e., obese persons with few or no metabolic abnormalities. So far, associations between MHO and coronary artery calcification (CAC), a measure of subclinical atherosclerosis, have mainly been studied cross-sectionally in Asian populations. We assessed cross-sectional and longitudinal MHO CAC associations in a Caucasian population.

Epidemiology of bacteria and viruses in the respiratory tract of humans and domestic pigs

Bacteria and viruses were analysed in the upper respiratory tract of symptomatic pig farmers and their domestic pigs. Eighty six human nasal and 495 (50 pools) porcine snout swabs were collected in Schleswig-Holstein, Germany. Staphylococcus (S.) aureus (62.8%, 54/86), human rhino- and coronaviruses (HRV, 29.1%, 25/86; HCoV, 16.3%, 14/86) were frequently detected in humans, while Haemophilus parasuis (90.0%, 45/50), Mycoplasma hyorhinis (78.6%, 11/14), Enterovirus G (EV-G, 56.0%, 28/50) and S. aureus (36.0%, 18/50), respectively, were highly prevalent in pigs. The detection of S. aureus in human follow-up samples indicates a carrier status. The methicillin-resistant phenotype (MRSA) was identified in 33.3% (18/54) of nasal swabs and in one of 18 (5.6%) pooled snout swabs that were tested positive for S. aureus. Strains were indicative of the livestock-associated clonal complex CC398, with t011 being the most common staphylococcal protein A type. Enterobacterales and non-fermenters were frequently isolated from swabs. Their detection in follow-up samples suggests a carrier status. All were classified as being non-multiresistant. There was no example for cross-species transmission of viruses. In contrast, transmission of S. aureus through occupational contact to pigs seems possible. The study contributes to the ‘One Health’ approach.     

The prevalence of chronic low back pain and lumbar deformities in patients with Parkinson’s disease: implications on spinal surgery

Purpose

This observational study was aimed at quantification of low back pain (LBP) in Parkinsonian patients and its morphological correlation.

Background

Parkinson’s disease (PD) is a common disabling condition in the elderly population. Parkinsonian patients frequently are troubled by LBP. Causes for LBP in PD are muscular imbalances by the movement disorder itself and skeletal degeneration.

Methods

Ninety-seven PD patients and 97 controls were inquired about low back pain through the Oswestry Low Back Pain Disability Questionnaire and visual analogue scales. Fifty-four patients with LBP underwent X-ray of the lumbar spine in two planes and flexion–extension views. Parkinson’s disease was characterized by stage, disease duration, motor score, lateralization of symptoms and dosage of medication.

Results

LBP occurred significantly more frequent in PD (87.6%) compared to controls (62.6%) with longer duration and higher pain intensity. Pain intensity and disability scores were associated with higher PD stages and higher motor scores. Patients with the hypokinetic PD subtype experienced more pain intensity. X-ray of the lumbar spine revealed lumbar arthrosis in 79.6%, scoliosis in 38.8% and spondylolisthesis in 24.1% of PD patients with LBP. Lateralization of scoliosis and PD symptoms were significantly correlated. Only a small portion of PD patients with LBP received specialized orthopaedic treatment.

Conclusion

LBP and lumbar degeneration are common in PD. Both are related to movement disorder symptoms. The knowledge about musculoskeletal conditions in Parkinson’s disease is important for an interdisciplinary conservative or operative treatment decision of LBP.

Graphical abstract

These slides can be retrieved under Electronic Supplementary Material.

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Diagnostic red flags: steroid‐treated malignant CNS lymphoma mimicking autoimmune inflammatory demyelination

The presence of inflammation and demyelination in a central nervous system (CNS) biopsy points towards a limited, yet heterogeneous group of pathologies, of which multiple sclerosis (MS) represents one of the principal considerations. Inflammatory demyelination has also been reported in patients with clinically suspected primary central nervous system lymphoma (PCNSL), especially when steroids had been administered prior to biopsy acquisition. The histopathological changes induced by corticosteroid treatment can range from mild reduction to complete disappearance of lymphoma cells. It has been proposed that in the absence of neoplastic B cells, these biopsies are indistinguishable from MS, yet despite the clinical relevance, no histological studies have specifically compared the two entities. In this work, we analyzed CNS biopsies from eight patients with inflammatory demyelination in whom PCNSL was later histologically confirmed, and compared them with nine well defined early active multiple sclerosis lesions. In the patients with steroid‐treated PCNSL (ST‐PCNSL) the interval between first and second biopsy ranged from 3 to 32 weeks; all of the patients had received corticosteroids before the first, but not the second biopsy. ST‐PCNSL patients were older than MS patients (mean age: ST‐PCNSL: 62 ± 4 years, MS: 30 ± 2 years), and histological analysis revealed numerous apoptoses, patchy and incomplete rather than confluent and complete demyelination and a fuzzy lesion edge. The loss of Luxol fast blue histochemistry was more profound than that of myelin proteins in immunohistochemistry, and T cell infiltration in ST‐PCNSL exceeded that in MS by around fivefold (P = 0.005). Our data indicate that in the presence of extensive inflammation and incomplete, inhomogeneous demyelination, the neuropathologist should refrain from primarily considering autoimmune inflammatory demyelination and, even in the absence of lymphoma cells, instigate close clinical follow‐up of the patient to detect recurrent lymphoma.     

Association of coronary artery calcium and congestive heart failure in the general population: results of the Heinz Nixdorf Recall Study

Background

The main causes of congestive heart failure (CHF) are coronary artery disease (CAD) and arterial hypertension. Coronary artery calcification (CAC) evidencing coronary atherosclerosis may occur prior to clinical CAD. The aim of our study was to assess the association between CAC as a sign of subclinical CAD and CHF in a general unselected population.

Methods

Participants of the Heinz Nixdorf Recall Study without known CAD but with known CHF as defined by a physicians’ diagnosis of CHF and dyspnea were identified. B-natriuretic peptide was measured and an exercise stress test was performed as possible. Cardiovascular risk factors and the EBCT-based CAC Agatston score were determined.

Results

Those 105/4,230 subjects (2.5%) with CHF (age 65 ± 7 years, 44% males), had higher brain natriuretic peptide (BNP) levels (median BNP 36.8 [16.5–70.1] vs. 17.6 [9.5–31.7] pg/ml, p < 0.01) and lower exercise capacity (108.7 ± 39.4 vs. 130.0 ± 40.7 W, p < 0.01) than those without. CAC in subjects with CHF was significantly higher than in those without (median CAC 64.7 [8.5–312.3] vs. 11.6 [0–109.8], p < 0.01). In univariate analysis, CAC-burden after logarithmic transformation according to log₂(CAC + 1) showed a significant association with the presence of CHF (odds ratio (OR) (95% CI): 1.16 (1.1–1.23), p < 0.0001). Adjustment for age and sex (OR 1.11 (1.04–1.18), p < 0.001), additional Framingham risk score (OR 1.09 (1.02–1.16), p = 0.015), and additional cardiovascular medication (OR 1.07 (0.998–1.14), p = 0.058) attenuated this association. Age, systolic blood pressure, antihypertensive medication and increased body mass index also remained significantly associated with presence of CHF in the full multivariate model.

Conclusion

The observed association between CAC and CHF in persons without clinically overt CAD is partly determined by risk factors that are involved in the natural history of both CAC and CHF. Whether CAC has a role to identify subjects at risk of future CHF remains to be determined using follow-up analyses.